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Updated: Mar 16, 2026
Isolation, Transfection, and Culture of Primary Human Monocytes
Published on: December 16, 2019
Lipopolysaccharide suppresses human immunodeficiency virus 1 reverse transcription in macrophages
Feng-Liang Liu1, Jia-Wu Zhu1,2, Dan Mu1,2
1Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, 650223, Yunnan, China.
Abstract:
HIV-1-infected macrophages are long-lived and act as human immunodeficiency virus 1 (HIV-1) virus reservoirs. Lipopolysaccharide (LPS) has been demonstrated to suppress HIV-1 replication in macrophages, but the mechanism is not clear. Previous research suggested that downregulation of CD4 and CCR5 as well as blockage of the interaction of HIV-1 with cells are major causes of inhibition of HIV-1 replication in macrophages by LPS. In order to study whether LPS blocks the post-entry event of HIV-1 replication, we developed a macrophage HIV-1 infection model by using VSV-G pseudotyped HIV-1-luciferase virus to infect THP-1 differentiated macrophage-like cells. We found that LPS can suppress HIV-1 replication at post-entry steps. Further study suggested that HIV-1 reverse transcription was blocked by LPS, but addition of exogenous deoxyribonucleosides led to only partial recovery of HIV-1 replication. However, the inhibition of pro-inflammatory pathway completely rescued HIV-1 replication. Thus, our study shows that LPS can suppress the events of HIV-1 replication post-entry, including reverse transcription, and this restriction is mediated by more than one mechanism.
Insights
Lipopolysaccharide (LPS) suppresses human immunodeficiency virus 1 (HIV-1) replication in macrophages post-entry. This restriction involves blocking reverse transcription and is mediated by multiple mechanisms, including the pro-inflammatory pathway.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Macrophages are key reservoirs for human immunodeficiency virus 1 (HIV-1).
- Lipopolysaccharide (LPS) is known to suppress HIV-1 replication in macrophages, but the underlying mechanisms remain unclear.
- Previous hypotheses suggested LPS inhibits HIV-1 by downregulating CD4/CCR5 or blocking viral entry.
Purpose of the Study:
- To investigate if LPS inhibits HIV-1 replication at post-entry stages.
- To elucidate the specific mechanisms by which LPS restricts HIV-1 replication in macrophages.
Main Methods:
- Development of a macrophage HIV-1 infection model using VSV-G pseudotyped HIV-1-luciferase virus.
- Infection of THP-1 differentiated macrophage-like cells with the engineered virus.
- Assessment of HIV-1 replication following LPS treatment, including reverse transcription assays and manipulation of pro-inflammatory pathways.
Main Results:
- LPS significantly suppresses HIV-1 replication at post-entry steps in macrophages.
- HIV-1 reverse transcription is a key target of LPS-mediated inhibition.
- While exogenous deoxyribonucleosides partially restored replication, complete rescue was achieved by inhibiting the pro-inflammatory pathway.
Conclusions:
- LPS exerts its inhibitory effect on HIV-1 post-entry, targeting reverse transcription.
- Multiple mechanisms contribute to LPS-induced restriction of HIV-1 replication, including modulation of the pro-inflammatory pathway.
- This study clarifies the complex interplay between LPS, macrophages, and HIV-1 replication.
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